ABSTRACT

The cardiac late sodium current (I_Na,late) is the small sustained component of the sodium current active during the plateau phase of the action potential. Several studies demonstrated that augmentation of the current can lead to cardiac arrhythmias; therefore, I_Na,late is considered as a promising antiarrhythmic target. Fundamentally, enlarged I_Na,late increases Na⁺ influx into the cell, which, in turn, is converted to elevated intracellular Ca²⁺ concentration through the Na⁺/Ca²⁺ exchanger. The excessive Ca²⁺ load is known to be proarrhythmic. This review describes the behavior of the voltage-gated Na⁺ channels generating I_Na,late in health and disease and aims to discuss the physiology and pathophysiology of Na⁺ and Ca²⁺ homeostasis in context with the enhanced I_Na,late demonstrating also the currently accessible antiarrhythmic choices.

 抽象的

心脏晚钠电流 (I _Na,late ) 是动作电位平台期期间活跃的钠电流的小持续分量。多项研究表明，电流增大会导致心律失常。因此，I _Na,late被认为是一个有前途的抗心律失常靶点。从根本上说，增大的 I _Na,late增加了 Na ⁺流入细胞，进而通过 Na ⁺ /Ca ²⁺交换器转化为升高的细胞内 Ca ²⁺浓度。已知过量的Ca ²⁺负荷会导致心律失常。本综述描述了电压门控 Na ⁺通道在健康和疾病_{后期产生 I Na}的行为，旨在讨论在 I Na 增强的背景下 Na ⁺和 Ca ²⁺稳态的生理学和病理生理学_，后期还证明了目前可用的抗心律失常选择。